Epilepsia Partialis continua secondary to diabetic ketoacidosis

Abstract Epilepsia partialis continua is a rare epileptic syndrome presenting with simple, partial, repetitive motor seizures. It can be a result of structural central nervous system lesion or due to metabolic causes. We report a case of a 65‐year‐old male patient diagnosed with EPC secondary to diabetic ketoacidosis.


| INTRODUCTION
Epilepsia partialis continua (EPC) is a disease characterized by simple partial motor seizures that are limited to a one part of the body in the form of repetitive regular or irregular clonic jerks without loss of consciousness. 1 EPC is a rare disease, with an estimated prevalence of one per million in the United Kingdom. 2 Additionally, EPC is reported to be more common among males. 3 EPC can occur as a result of structural damage, neoplasia, cortical dysplasia, metabolic abnormalities, or infection. 4 Seizures can continue for days, weeks, or potentially years, remaining localized to a single part of the body. 1 EPC management is in the form of antiepileptics as well as identification and treatment of the underlying cause. 5 Diabetes mellitus (DM) can cause central nervous system (CNS) complications, in form of cognitive dysfunction, metabolic and vascular complications. Regarding cognitive impairment, DM was reported to be associated with Alzheimer's disease. 6,7 In addition, patients with DM have a higher risk of stroke (2.5-3.5 times) when compared to non-diabetic individuals. 8 In terms of metabolic consequences, hypoglycemia causes a range of symptoms-ranging from cognitive impairment to coma and brain damage. 9 Finally, non-ketotic hyperglycemic status (NKH) and diabetic ketoacidosis (DKA) were reported to be causes of EPC. 1,10 However, the occurrence of EPC in patients with DKA is a rare phenomenon. [10][11][12] We present a case report of EPC secondary to diabetic ketoacidosis.

| CASE PRESENTATION
A 65-year-old male patient presented to the emergency department due to involuntary and repetitive episodes of the left upper limb movement for 2 days. These episodes consisted of continuous clonic movement of the left elbow, left wrist, and fingers of the left hand. Seizures had been occurring every 2-5 h, continuing for one to 3 min in each episode. To add, consciousness and sphincter control were preserved throughout the episodes. The patient denied a history of similar symptoms or epilepsy.
The patient looked unwell, temperature was 37.2°C, pulse rate was 98 beats per minute, respiratory rate was 28 cycles per minute, and blood pressure was 100/70 mmHg. In addition, the patient was thirsty with dry lips and mouth. The neurological examination of the patient was normal.
Based on the presentation, central nervous system lesions and electrolyte abnormalities were considered as a differential diagnosis. Based on that, laboratory investigations, magnetic resonance imaging (MRI), cerebrospinal fluid (CSF) study, and an electroencephalogram (EEG) were ordered. Laboratory investigations revealed a glucose level of 330 mg/dL (normal value: 70-100 mg/dL) and ketone bodies in the urine (three crosses). An arterial blood gas (ABG) test was consistent with metabolic acidosis (Ph: 7.24, pCO 2  The MRI (Figure 1), CSF, and EEG were of normal study. Based on that, the diagnosis of EPC was established.
The patients' diabetic ketoacidosis was treated by rehydration and correction of blood glucose. Additionally, sodium valproate was commenced, which adequately controlled the seizures. The patient was discharged 2 days later following the complete resolution of seizures and diabetic ketoacidosis. The list of discharge medications includes metformin and sodium valproate. The patient was referred to an endocrinologist for further follow-up of DM. Three months later, upon subsequent follow-up the patient did not suffer any following seizures.

| DISCUSSION
EPC is characterized by repeated clonic muscular contractions confined to a single body part at a regular short intervals, persisting for days or weeks. 13 Rarely hyperglycemia may lead to seizure, such as in cases of NKH. However, it is very rare in cases of DKA. 14 There are only three case reports of EPC in patients with ketotic hyperglycemia.
In hyperglycemic crises, hyperglycemia may lower the gamma-aminobutyric acid (GABA) levels, an inhibitory neurotransmitter, lowering the seizure threshold, and thus, explaining the occurrence of EPC. 15 It is important to mention that ketosis and acidosis increase the seizure threshold; thus, seizures are not common in DKA. 16 In our case, DKA was the first presentation of the DM. In addition, the MRI and CSF were normal. This is consistent with Van et al case report of EPC in a patient with DKA. 10 In another case report of EPC with DKA, however, MRI showed hypointense lesions in the white matter below the left precentral gyrus which upon follow-up imaging became hyperintense . 14 Authors attributed this to gliosis. 14 A previous study stated that mild focal gliosis may occur after a seizure. 17

| CONCLUSION
This report highlighted the association between EPC and diabetic ketoacidosis. Investigating metabolic disorders is an important part of assessing seizures, as EPC is resistant to anti-epileptic as a sole treatment, detecting and treating the underlying cause is a cornerstone aspect of management.

ACKNOWLEDGMENT
We would like to thank the patient for giving us the consent to report this important case.

CONFLICT OF INTEREST
The authors declare no conflict of interest. This case report did not receive any form of funding.

DATA AVAILABILITY STATEMENT
The data that support the findings of this study are available from the corresponding author upon reasonable request.

ETHICAL APPROVAL
Patient confidentiality was maintained in this report, and all ethical considerations were done in accordance with the Declaration of Helsinki.

CONSENT
A written informed consent was obtained from the patient prior to the writing and submission of this case report.